Infection of owl monkey kidney cells with Herpesvirus saimiri (HVS) induces the formation of a unique DNA polymerase with a molecular weight of about 190,000. The enzyme can be distinguished from the normal DNA polymerase by its template specificity for high G plus C, its requirement for high salt and by its relative insensitivity to heat and high pH. The HVS-induced enzyme is resistant to the DNA polymerase inhibitor phosphonoacetic acid, while the DNA polymerase induced by herpes simplex is substantially inhibited by this drug. The G plus C preferential template specificity of the HVS polymerase may suggest a mechanism for the generation and preferential selection of defective HVS DNA. Friend leukemia cell (FLC) lines exhibited increased intracellular heme levels when incubated with DMSO or butyric acid alone, but no increase when these inducers were added together. DMSO increased the rate of butyrate uptake into soluble and acid-insoluble fractions of FLC. Procaine inhibited the stimulatory effect of butyrate. Porphyrin accumulation was considerably greater in DMSO-induced FLC than in butyrate-stimulated cells. These differential and opposing effects of DMSO and butyrate on hemoglobin production suggest that these compounds have different modes of action. BIBLIOGRAPHIC REFERENCES: Bloomer, J.R., Bonkowsky, H.L., Ebert, P.S. and Mahoney, M.J.: Inheritance in protoporphyria. Comparison of heme synthetase activity in skin fibroblasts with clinical features. Lancet 31: 226-228, 1976. Ebert, P.S. and Buell, D.N.: Viral reverse transcriptase suppression associated with erythroid differentiation of Friend leukemia cells. J. Natl. Cancer Inst. 58: 635-640, 1977.